Blockade of IL-6 signal increases the susceptibility of renal cell carcinoma to interferon

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462492
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Fukushima Medical University
• Principal Investigator: Ishibashi Kei 福島県立医科大学, 医学部, 准教授 (90347211)
• Co-Investigator(Kenkyū-buntansha): KOJIMA Yoshiyuki 福島県立医科大学, 医学部, 教授 (60305539)
• Co-Investigator(Renkei-kenkyūsha): AIKAWA Ken 福島県立医科大学, 医学部, 准教授 (80295419) ; YANAGIDA Tomohiko 福島県立医科大学, 医学部, 講師 (20363765) ; HAGA Nobuhiro 福島県立医科大学, 医学部, 助教 (50586617)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 腎癌 / サイトカイン / TRAIL

Outline of Final Research Achievements

The effectiveness of a new strategy against human renal cell carcinomas (RCCs) that modifies interleukin (IL)-6 signaling was investigated in vitro and in vivo. In RCC cell lines, interferon (IFN)-α alters the autocrine production of the proinflammatory cytokine IL-6. The growth inhibitory effects of IFN-α under IL-6R knockdown conditions by tocilizumab were demonstrated by MTT assay. The in vivo effects of injections of tocilizumab and IFN administration were evaluated in groups of nude mice bearing s.c. xenografts of 786-0. The growth of the tumors in mice receiving combination therapy with tocilizumab and IFN-α was significantly suppressed in comparison with those in the tocilizumab, IFN-α and non-treated groups.TRAIL was up-regurated in the tumors which were treated with combination therapy with tocilizumab and IFN.

Free Research Field

腎癌